SAG101 Forms a Ternary Complex with EDS1 and PAD4 and Is Required for Resistance Signaling against Turnip Crinkle Virus

PLoS Pathogens

Rae-Dong Jeong¹  Aardra Kachroo¹  Pradeep Kachroo¹  Shifeng Zhu¹  Ludmila Lapchyk¹  Srivathsa C. Venugopal¹  DuRoy Navarre² 

[1] Department of Plant Pathology, University of Kentucky, Lexington, Kentucky, United States of America;U.S. Department of Agriculture–Agricultural Research Service, Washington State University, Prosser, Washington, United States of America

关键词: Leaves;    Genetically modified plants;    Protein extraction;    Arabidopsis thaliana;    Protein interactions;    Protein expression;    Reverse transcriptase-polymerase chain reaction;    Immune system proteins;   

DOI  :  10.1371/journal.ppat.1002318

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

EDS1, PAD4, and SAG101 are common regulators of plant immunity against many pathogens. EDS1 interacts with both PAD4 and SAG101 but direct interaction between PAD4 and SAG101 has not been detected, leading to the suggestion that the EDS1-PAD4 and EDS1-SAG101 complexes are distinct. We show that EDS1, PAD4, and SAG101 are present in a single complex in planta. While this complex is preferentially nuclear localized, it can be redirected to the cytoplasm in the presence of an extranuclear form of EDS1. PAD4 and SAG101 can in turn, regulate the subcellular localization of EDS1. We also show that the Arabidopsis genome encodes two functionally redundant isoforms of EDS1, either of which can form ternary complexes with PAD4 and SAG101. Simultaneous mutations in both EDS1 isoforms are essential to abrogate resistance (R) protein-mediated defense against turnip crinkle virus (TCV) as well as avrRps4 expressing Pseudomonas syringae. Interestingly, unlike its function as a PAD4 substitute in bacterial resistance, SAG101 is required for R-mediated resistance to TCV, thus implicating a role for the ternary complex in this defense response. However, only EDS1 is required for HRT-mediated HR to TCV, while only PAD4 is required for SA-dependent induction of HRT. Together, these results suggest that EDS1, PAD4 and SAG101 also perform independent functions in HRT-mediated resistance.

【 授权许可】

CC BY